Author(s): Yang CS, Teeple M, Muglia J, Robinson-Bostom L
A switch from cell-mediated to humoral immunity (helper T 1 [Th1] to helper T 2 [Th2] shift) during gestation plays a key role in placental immune tolerance. As a result, skin diseases that are Th2 mediated often worsen, whereas skin diseases that are Th1 mediated often improve during gestation. Also, due to fluctuations in glandular activity, skin diseases involving sebaceous and eccrine glands may flare, whereas those involving apocrine glands may improve during pregnancy. Despite these trends, inflammatory and glandular skin diseases do not always follow the predicted pattern, and courses are often diverse. We review the gestational course of inflammatory skin diseases, such as atopic dermatitis (atopic eruption of pregnancy), psoriasis, impetigo herpetiformis, urticaria, erythema annulare centrifugum, pityriasis rosea, sarcoidosis, Sweet syndrome, and erythema nodosum, as well as glandular skin diseases, including acne vulgaris, acne rosacea, perioral dermatitis, hidradenitis suppurativa, Fox-Fordyce disease, hyperhidrosis, and miliaria. For each of these diseases, we discuss the pathogenesis, clinical presentation, and management with special consideration for maternal and fetal safety.
Dermatology Journal and/or Publisher
Journal Name: Clinics in dermatology
Journal Abbreviation: Clin. Dermatol.
Journal Date Published: 2016-06-06
National Center for Biotechnology Information
Article Source: http://www.ncbi.nlm.nih.gov/pubmed/27265071
Lasted Revision: 2017-05-03
Abstract Source: National Center for Biotechnology Information, U.S. National Library of Medicine Abstract Query for Hidradenitis suppurativa (HS).